Under normal conditions the brain is almost totally dependent upon the oxidation of glucose for its energy requirements. Thiamine is known to be an important coenzyme in normal brain glucose oxidation. Several competing theories have been proposed to explain the neurological symptoms of thiamine deficiency, one of which is that symptoms result from a defect in the oxidation of glucose as a consequence of the coenzyme function of thiamine. Recently an autoradiographic method has been developed by Sokoloff and his colleagues for the quantitative measurement of local cerebral glucose utilization in vivo using (14 C) 2-deoxyglucose. The objective of this study is to use the (14 C) 2-deoxyglucose method to determine whether local cerebral glucose utilization decreases during thiamine deficiency cause the neurological symptoms of thiamine deficiency. Changes of local cerebral glucose utilization will be correlated with neurological symptoms of dietary thiamine deficiency and with recovery of symptoms after administration of thiamine. The study will attempt to describe changes of local cerebral glucose utilization which could be related to the memory disorder of the Korsakoff's amnestic syndrome.